Browsing by Subject "Skeletal muscles"

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    Fast in vivo 23 Na imaging and T2∗ mapping using accelerated 2D-FID UTE magnetic resonance spectroscopic imaging at 3 T: Proof of concept and reliability study
    (Wiley, 2021) Alhulail, Ahmad A.; Xia, Pingyu; Shen, Xin; Nichols, Miranda; Volety, Srijyotsna; Farley, Nicholas; Thomas, Michael Albert; Nagel, Armin M.; Dydak, Ulrike; Emir, Uzay E.; Radiology and Imaging Sciences, School of Medicine
    Purpose: To implement an accelerated MR-acquisition method allowing to map T2* relaxation and absolute concentration of sodium within skeletal muscles at 3T. Methods: A fast-UTE-2D density-weighted concentric-ring-trajectory 23 Na-MRSI technique was used to acquire 64 time points of FID with a spectral bandwidth of 312.5 Hz with an in-plane resolution of 2.5 × 2.5 mm2 in ~15 min. The fast-relaxing 23 Na signal was localized with a single-shot, inversion-recovery-based, non-echo (SIRENE) outer volume suppression (OVS) method. The sequence was verified using simulation and phantom studies before implementing it in human calf muscles. To evaluate the 2D-SIRENE-MRSI (UTE = 0.55 ms) imaging performance, it was compared to a 3D-MRI (UTE = 0.3 ms) sequence. Both data sets were acquired within 2 same-day sessions to assess repeatability. The T2* values were fitted voxel-by-voxel using a biexponential model for the 2D-MRSI data. Finally, intra-subject coefficients of variation (CV) were estimated. Results: The MRSI-FID data allowed us to map the fast and slow components of T2* in the calf muscles. The spatial distributions of 23 Na concentration for both MRSI and 3D-MRI acquisitions were significantly correlated (P < .001). The test-retest analysis rendered high repeatability for MRSI with a CV of 5%. The mean T2* Fast in muscles was 0.7 ± 0.1 ms (contribution fraction = 37%), whereas T2* Slow was 13.2 ± 0.2 ms (63%). The mean absolute muscle 23 Na concentration calculated from the T2* -corrected data was 28.6 ± 3.3 mM. Conclusion: The proposed MRSI technique is a reliable technique to map sodium's absolute concentration and T2* within a clinically acceptable scan time at 3T.
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    Skeletal Muscle Regeneration and Oxidative Stress Are Altered in Chronic Kidney Disease
    (Plos, 2016-08-03) Avin, Keith G.; Chen, Neal X.; Organ, Jason M.; Zarse, Chad; O'Neil, Kalisha; Conway, Richard G.; Konrad, Robert J.; Bacallao, Robert L.; Allen, Matthew R.; Moe, Sharon M.; Department of Physical Therapy, School of Health and Rehabilitation Sciences
    Skeletal muscle atrophy and impaired muscle function are associated with lower health-related quality of life, and greater disability and mortality risk in those with chronic kidney disease (CKD). However, the pathogenesis of skeletal dysfunction in CKD is unknown. We used a slow progressing, naturally occurring, CKD rat model (Cy/+ rat) with hormonal abnormalities consistent with clinical presentations of CKD to study skeletal muscle signaling. The CKD rats demonstrated augmented skeletal muscle regeneration with higher activation and differentiation signals in muscle cells (i.e. lower Pax-7; higher MyoD and myogenin RNA expression). However, there was also higher expression of proteolytic markers (Atrogin-1 and MuRF-1) in CKD muscle relative to normal. CKD animals had higher indices of oxidative stress compared to normal, evident by elevated plasma levels of an oxidative stress marker, 8-hydroxy-2' -deoxyguanosine (8-OHdG), increased muscle expression of succinate dehydrogenase (SDH) and Nox4 and altered mitochondria morphology. Furthermore, we show significantly higher serum levels of myostatin and expression of myostatin in skeletal muscle of CKD animals compared to normal. Taken together, these data show aberrant regeneration and proteolytic signaling that is associated with oxidative stress and high levels of myostatin in the setting of CKD. These changes likely play a role in the compromised skeletal muscle function that exists in CKD.